Normal mesenchymal stem cells can improve the abnormal function of T cells in psoriasis via upregulating transforming growth factor‐β receptor

• Published in: Journal of dermatology 2022-10, Vol.49 (10), p.988-997
• Main Authors: Jiao, Juanjuan, Zhao, Xincheng, Wang, Ying, Liang, Nannan, Li, Juan, Yang, Xiaohong, Xing, Jianxiao, Zhou, Ling, Li, Junqin, Hou, Ruixia, Li, Xinhua, Zhang, Kaiming
• Format: Article
• Language: English
• Subjects: Apoptosis; CD3 antigen; CD3+ T cells; Cell culture; Cell differentiation; Cell proliferation; dermal mesenchymal stromal cells; Effector cells; Flow cytometry; Growth factors; Helper cells; Immunoregulation; Immunosuppression; immunosuppressive; Lymphocytes; Lymphocytes T; Mesenchymal stem cells; Psoriasis; Skin diseases; Smad protein; Stem cells; Stromal cells; Transforming growth factor-b; transforming growth factor‐β receptors; Western blotting
• ISSN: 0385-2407; 1346-8138
• DOI: 10.1111/1346-8138.16490

Psoriasis, a chronic inflammatory skin disease, is a refractory disorder. Previous studies have shown that the imbalance of the T‐helper (Th)17/regulatory T cells (Treg) results in the immune imbalance of T cells in psoriatic patients, and that mesenchymal stem cells display an immunosuppressive role by promoting the differentiation of T cells into Treg, leading to a reduction in the proportion of Th17/Treg. Utility of mesenchymal stem cells is becoming a new approach for the treatment of immune disorders. Following co‐culture of dermal mesenchymal stromal cells (DMSC) and CD3+ T cells with or without transforming growth factor (TGF)‐β receptor inhibitor, the biological function and relative signal pathway of CD3+ T cells were assessed by flow cytometry, transwell, real‐time polymerase chain reaction and western blotting, respectively. Normal DMSC were more potent than psoriatic DMSC in inhibition of CD3+ T‐cell proliferation, and stimulation of CD3+ T‐cell apoptosis than psoriasis DMSC. Moreover, normal DMSC decreased the ratio of Th17/Treg, while enhancing the immunosuppressive effect of Tregs on effector T cells. However, TGF‐β receptor (TGF‐βR) inhibitor attenuated the effect of normal DMSC on CD3+ T cells and Th17/Treg ratio. Additionally, the normal DMSC were more potent than the psoriatic DMSC in increasing TGF‐β receptors and activation of TGF‐β/SMAD pathway in psoriatic CD3+ T cells. In conclusion, normal DMSC can partially improve the biological function and immunosuppressive ability of psoriatic CD3+ T cells, possibly via upregulating the TGF‐β receptors.